622 Baseline inflammatory indexes and clinicopathological features to predict the outcome of acute interstitial nephritis
Abstract Backgrounds-and-aims Acute tubulointerstitial nephritis(AIN) is a rare cause of acute kidney injury(AKI). We aimed to investigate the characteristics of AIN patients and predictive factors for treatment response. Method 31 patients diagnosed with AIN by biopsy between 2006-2021 were include...
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| description | Abstract
Backgrounds-and-aims
Acute tubulointerstitial nephritis(AIN) is a rare cause of acute kidney injury(AKI). We aimed to investigate the characteristics of AIN patients and predictive factors for treatment response.
Method
31 patients diagnosed with AIN by biopsy between 2006-2021 were included in this retrospective study. Baseline clinical, pathological, and laboratory findings, including CBC(complete blood count), creatinine, serum-immune-inflammation-index(SII), neutrophil-to-lymphocyte ratio(NLR), and platelet-to-lymphocyte ratio(PLR) were evaluated. Also, treatment response and creatinine levels at the last follow-up were noted.
Results
Median age was 46 years, and 80.6% of the patients were female. Median baseline creatinine and proteinuria levels were 4.1 mg/dL and 0.84 g/g or g/day. Median follow-up was 14 months. 93.5% of patients received immunosuppressives. End-stage-kidney-disease(ESKD) developed in five patients. Renal recovery(creatinine < 1.4 mg/dL) was observed in 17 (54.8%) patients. Global glomerulosclerosis percentage, interstitial fibrosis(IF), tubular atrophy(TA), granuloma formation, and higher baseline hemoglobin levels were associated with poor renal outcomes(non-responder). Also, ESKD-developed patients had higher baseline hemoglobin(p = 0.033) and lymphocyte(p = 0.044) and lower PLR levels(p = 0.016), as well as higher degrees of global glomerulosclerosis(p = 0.014), IF(p = 0.042), and TA(p = 0.030).
Conclusion
Treatment rates are low for AIN, which may lead to ESKD. Besides chronicity in pathology specimens, higher baseline hemoglobin levels and lower PLR might be prognostic for AIN. Further studies should be conducted on new markers for AIN.
Table:
Baseline clinical/laboratory/pathology and treatment data of responder(last serum creatinine < 1.4 mg/dL) and non-responder groups.
No Response
Responder
Parameters
(n = 14)
(n = 17)
p-value
Age, median (min-max)
44 (21-61)
44.5 (17-71)
0.874
Sex, F/M
10/4
15/2
0.370
Creatinine (mg/dl)
3.8 (2.4-9.1)
4.32 (1.03-11.2)
0.677
eGFR (CKD-EPI)
16.9 (4.7-32)
11.29 (3.69-70)
0.525
Albumin, mean ± std
3.9 ± 0.8
4.0 ± 0.4
0.573
Hgb
11.8 (6.9-13.8)
9.75 (7.2-11.7)
0.029
Lymph
1400 (400-3300)
1180 (500-1700)
0.140
Neutroph
6500 (3100-24700)
5650 (3270-9900)
0.665
Plt
280000 (75000-645000)
291500 (148600-507000)
0.733
Eos
200 (0-700)
135 (0-300)
0.151
SII
1400 (513.6-5689.8)
1635 (495.7-4563)
0.603
NLR
4.88 (2.3-17.6)
4.97 (2.6-12.6)
0.603
PLR
194.3 (124.2-1123.5)
302.26 (151.6-460.9)
0.225
P |
| doi_str_mv | 10.1093/ndt/gfae069.420 |
| format | Article |
| fullrecord | <record><control><sourceid>oup_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1093_ndt_gfae069_420</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/ndt/gfae069.420</oup_id><sourcerecordid>10.1093/ndt/gfae069.420</sourcerecordid><originalsourceid>FETCH-LOGICAL-c1160-212a1f327bdf1e63ffd29b2cd364adaa6e51e2dadab6a0ec1379c1a36ec2d5bc3</originalsourceid><addsrcrecordid>eNqFkEtPwzAQhC0EEqVw5uozUlo_EoccoeIlVeIC52hjr1ujJI5sR6L_HlftndPOamdGq4-Qe85WnDVyPZq03llApppVKdgFWfBSsULIx-qSLLKDF6xizTW5ifGHMdaIul6QgxKCPkPE3o1I3Wh7GAZIPhzyYvAXI4XRUJ3PTvsJ0t73fuc09NQipDlkQ_J0CmicTjTtkfo5aT_kaSnoOR1bE4aYXHI5NeK0D1nGW3JloY94d55L8v368rV5L7afbx-bp22hOT_-zwVwK0XdGctRSWuNaDqhjVQlGACFFUdhsuwUMNRc1o3mIBVqYapOyyVZn3p18DEGtO0U3ADh0HLWHsm1mVx7JtdmcjnxcEr4efrX_AdR9XVz</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>622 Baseline inflammatory indexes and clinicopathological features to predict the outcome of acute interstitial nephritis</title><source>OUP_牛津大学出版社现刊</source><creator>Dirim, Ahmet Burak ; Namazova, Nazrin ; Dirim, Merve Guzel ; Oto, Ozgur Akin ; Artan, Ayse Serra ; Hurdogan, Ozge ; Ozluk, Yasemin ; Yazici, Halil</creator><creatorcontrib>Dirim, Ahmet Burak ; Namazova, Nazrin ; Dirim, Merve Guzel ; Oto, Ozgur Akin ; Artan, Ayse Serra ; Hurdogan, Ozge ; Ozluk, Yasemin ; Yazici, Halil</creatorcontrib><description>Abstract
Backgrounds-and-aims
Acute tubulointerstitial nephritis(AIN) is a rare cause of acute kidney injury(AKI). We aimed to investigate the characteristics of AIN patients and predictive factors for treatment response.
Method
31 patients diagnosed with AIN by biopsy between 2006-2021 were included in this retrospective study. Baseline clinical, pathological, and laboratory findings, including CBC(complete blood count), creatinine, serum-immune-inflammation-index(SII), neutrophil-to-lymphocyte ratio(NLR), and platelet-to-lymphocyte ratio(PLR) were evaluated. Also, treatment response and creatinine levels at the last follow-up were noted.
Results
Median age was 46 years, and 80.6% of the patients were female. Median baseline creatinine and proteinuria levels were 4.1 mg/dL and 0.84 g/g or g/day. Median follow-up was 14 months. 93.5% of patients received immunosuppressives. End-stage-kidney-disease(ESKD) developed in five patients. Renal recovery(creatinine < 1.4 mg/dL) was observed in 17 (54.8%) patients. Global glomerulosclerosis percentage, interstitial fibrosis(IF), tubular atrophy(TA), granuloma formation, and higher baseline hemoglobin levels were associated with poor renal outcomes(non-responder). Also, ESKD-developed patients had higher baseline hemoglobin(p = 0.033) and lymphocyte(p = 0.044) and lower PLR levels(p = 0.016), as well as higher degrees of global glomerulosclerosis(p = 0.014), IF(p = 0.042), and TA(p = 0.030).
Conclusion
Treatment rates are low for AIN, which may lead to ESKD. Besides chronicity in pathology specimens, higher baseline hemoglobin levels and lower PLR might be prognostic for AIN. Further studies should be conducted on new markers for AIN.
Table:
Baseline clinical/laboratory/pathology and treatment data of responder(last serum creatinine < 1.4 mg/dL) and non-responder groups.
No Response
Responder
Parameters
(n = 14)
(n = 17)
p-value
Age, median (min-max)
44 (21-61)
44.5 (17-71)
0.874
Sex, F/M
10/4
15/2
0.370
Creatinine (mg/dl)
3.8 (2.4-9.1)
4.32 (1.03-11.2)
0.677
eGFR (CKD-EPI)
16.9 (4.7-32)
11.29 (3.69-70)
0.525
Albumin, mean ± std
3.9 ± 0.8
4.0 ± 0.4
0.573
Hgb
11.8 (6.9-13.8)
9.75 (7.2-11.7)
0.029
Lymph
1400 (400-3300)
1180 (500-1700)
0.140
Neutroph
6500 (3100-24700)
5650 (3270-9900)
0.665
Plt
280000 (75000-645000)
291500 (148600-507000)
0.733
Eos
200 (0-700)
135 (0-300)
0.151
SII
1400 (513.6-5689.8)
1635 (495.7-4563)
0.603
NLR
4.88 (2.3-17.6)
4.97 (2.6-12.6)
0.603
PLR
194.3 (124.2-1123.5)
302.26 (151.6-460.9)
0.225
Proteinuria
0.84 (0-8)
0.84 (0-3)
0.766
Follow-up (months)
14 (1-52)
10.5 (2-168)
0.402
Treatments, (%)
Steroids, including pulse
(92.9)
(94.1)
1.000
AZA/MMF
(21.4)
(0)
0.304
Pulse-steroids
(28.6)
(17.6)
0.671
Hemodialysis-at-admission
(28.6)
(17.6)
0.671
AIN Etiology, (%)
Unknown, (50)
Unknown, (23.5)
0.153
NSAID, (14.3)
NSAID, (29.4)
0.412
Antibiotic, (7.1)
Antibiotic, (35.2)
0.094
Sarcoidosis, (21.4)
Sarcoidosis, (5.9)
0.304
Sjögren, (7.1)
Sjögren, (5.9)
1.000
Tubulitis, (%)
Not significant (NS)
(21.4)
(11.8)
0.467
Mild
(57.1)
(88.2)
Moderate
(7.1)
(0)
Severe
2 (14.3)
0 (0)
Lymphocytic infiltration, (%)
NS
(7.1)
(0)
0.452
Mild
(64.3)
(82.4)
Mod
(21.4)
(11.8)
Sev
(7.1)
(5.9)
Eosinophilic inf, (%)
NS
(57.1)
(52.9)
0.815
Mild
(21.4)
(88.2)
Mod
(7.1)
(5.9)
Sev
(14.3)
(11.8)
Plasmacytic inf, (%)
NS
(57.1)
(82.4)
0.124
Mild
(7.1)
(0)
Mod
(7.1)
(0)
Sev
(28.6)
(17.6)
Granuloma formation, (%)
No
(50)
(100)
0.012
Mild/microgranuloma
(28.6)
(0)
Moderate
(14.3)
(0)
Extensive
(7.1)
(0)
TA, (%)
NS
(28.6)
(76.5)
0.024
Mild
(64.3)
(23.5)
Mod
(7.1)
(0)
Sev
(0)
(0)
IF, (%)
NS
(57.1)
(94.1)
0.047
Mild
(35.7)
(5.9)
Mod
(7.1)
(0)
Sev
(0)
(0)
Global sclerotic glomeruli (%), median
(0-83.3)
(0-50)
0.013
Segmental sclerotic glomeruli (%), median
0 (0-9)
0 (0-0)
0.270</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfae069.420</identifier><language>eng</language><publisher>Oxford University Press</publisher><ispartof>Nephrology, dialysis, transplantation, 2024-05, Vol.39 (Supplement_1)</ispartof><rights>The Author(s) 2024. Published by Oxford University Press on behalf of the ERA. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids></links><search><creatorcontrib>Dirim, Ahmet Burak</creatorcontrib><creatorcontrib>Namazova, Nazrin</creatorcontrib><creatorcontrib>Dirim, Merve Guzel</creatorcontrib><creatorcontrib>Oto, Ozgur Akin</creatorcontrib><creatorcontrib>Artan, Ayse Serra</creatorcontrib><creatorcontrib>Hurdogan, Ozge</creatorcontrib><creatorcontrib>Ozluk, Yasemin</creatorcontrib><creatorcontrib>Yazici, Halil</creatorcontrib><title>622 Baseline inflammatory indexes and clinicopathological features to predict the outcome of acute interstitial nephritis</title><title>Nephrology, dialysis, transplantation</title><description>Abstract
Backgrounds-and-aims
Acute tubulointerstitial nephritis(AIN) is a rare cause of acute kidney injury(AKI). We aimed to investigate the characteristics of AIN patients and predictive factors for treatment response.
Method
31 patients diagnosed with AIN by biopsy between 2006-2021 were included in this retrospective study. Baseline clinical, pathological, and laboratory findings, including CBC(complete blood count), creatinine, serum-immune-inflammation-index(SII), neutrophil-to-lymphocyte ratio(NLR), and platelet-to-lymphocyte ratio(PLR) were evaluated. Also, treatment response and creatinine levels at the last follow-up were noted.
Results
Median age was 46 years, and 80.6% of the patients were female. Median baseline creatinine and proteinuria levels were 4.1 mg/dL and 0.84 g/g or g/day. Median follow-up was 14 months. 93.5% of patients received immunosuppressives. End-stage-kidney-disease(ESKD) developed in five patients. Renal recovery(creatinine < 1.4 mg/dL) was observed in 17 (54.8%) patients. Global glomerulosclerosis percentage, interstitial fibrosis(IF), tubular atrophy(TA), granuloma formation, and higher baseline hemoglobin levels were associated with poor renal outcomes(non-responder). Also, ESKD-developed patients had higher baseline hemoglobin(p = 0.033) and lymphocyte(p = 0.044) and lower PLR levels(p = 0.016), as well as higher degrees of global glomerulosclerosis(p = 0.014), IF(p = 0.042), and TA(p = 0.030).
Conclusion
Treatment rates are low for AIN, which may lead to ESKD. Besides chronicity in pathology specimens, higher baseline hemoglobin levels and lower PLR might be prognostic for AIN. Further studies should be conducted on new markers for AIN.
Table:
Baseline clinical/laboratory/pathology and treatment data of responder(last serum creatinine < 1.4 mg/dL) and non-responder groups.
No Response
Responder
Parameters
(n = 14)
(n = 17)
p-value
Age, median (min-max)
44 (21-61)
44.5 (17-71)
0.874
Sex, F/M
10/4
15/2
0.370
Creatinine (mg/dl)
3.8 (2.4-9.1)
4.32 (1.03-11.2)
0.677
eGFR (CKD-EPI)
16.9 (4.7-32)
11.29 (3.69-70)
0.525
Albumin, mean ± std
3.9 ± 0.8
4.0 ± 0.4
0.573
Hgb
11.8 (6.9-13.8)
9.75 (7.2-11.7)
0.029
Lymph
1400 (400-3300)
1180 (500-1700)
0.140
Neutroph
6500 (3100-24700)
5650 (3270-9900)
0.665
Plt
280000 (75000-645000)
291500 (148600-507000)
0.733
Eos
200 (0-700)
135 (0-300)
0.151
SII
1400 (513.6-5689.8)
1635 (495.7-4563)
0.603
NLR
4.88 (2.3-17.6)
4.97 (2.6-12.6)
0.603
PLR
194.3 (124.2-1123.5)
302.26 (151.6-460.9)
0.225
Proteinuria
0.84 (0-8)
0.84 (0-3)
0.766
Follow-up (months)
14 (1-52)
10.5 (2-168)
0.402
Treatments, (%)
Steroids, including pulse
(92.9)
(94.1)
1.000
AZA/MMF
(21.4)
(0)
0.304
Pulse-steroids
(28.6)
(17.6)
0.671
Hemodialysis-at-admission
(28.6)
(17.6)
0.671
AIN Etiology, (%)
Unknown, (50)
Unknown, (23.5)
0.153
NSAID, (14.3)
NSAID, (29.4)
0.412
Antibiotic, (7.1)
Antibiotic, (35.2)
0.094
Sarcoidosis, (21.4)
Sarcoidosis, (5.9)
0.304
Sjögren, (7.1)
Sjögren, (5.9)
1.000
Tubulitis, (%)
Not significant (NS)
(21.4)
(11.8)
0.467
Mild
(57.1)
(88.2)
Moderate
(7.1)
(0)
Severe
2 (14.3)
0 (0)
Lymphocytic infiltration, (%)
NS
(7.1)
(0)
0.452
Mild
(64.3)
(82.4)
Mod
(21.4)
(11.8)
Sev
(7.1)
(5.9)
Eosinophilic inf, (%)
NS
(57.1)
(52.9)
0.815
Mild
(21.4)
(88.2)
Mod
(7.1)
(5.9)
Sev
(14.3)
(11.8)
Plasmacytic inf, (%)
NS
(57.1)
(82.4)
0.124
Mild
(7.1)
(0)
Mod
(7.1)
(0)
Sev
(28.6)
(17.6)
Granuloma formation, (%)
No
(50)
(100)
0.012
Mild/microgranuloma
(28.6)
(0)
Moderate
(14.3)
(0)
Extensive
(7.1)
(0)
TA, (%)
NS
(28.6)
(76.5)
0.024
Mild
(64.3)
(23.5)
Mod
(7.1)
(0)
Sev
(0)
(0)
IF, (%)
NS
(57.1)
(94.1)
0.047
Mild
(35.7)
(5.9)
Mod
(7.1)
(0)
Sev
(0)
(0)
Global sclerotic glomeruli (%), median
(0-83.3)
(0-50)
0.013
Segmental sclerotic glomeruli (%), median
0 (0-9)
0 (0-0)
0.270</description><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNqFkEtPwzAQhC0EEqVw5uozUlo_EoccoeIlVeIC52hjr1ujJI5sR6L_HlftndPOamdGq4-Qe85WnDVyPZq03llApppVKdgFWfBSsULIx-qSLLKDF6xizTW5ifGHMdaIul6QgxKCPkPE3o1I3Wh7GAZIPhzyYvAXI4XRUJ3PTvsJ0t73fuc09NQipDlkQ_J0CmicTjTtkfo5aT_kaSnoOR1bE4aYXHI5NeK0D1nGW3JloY94d55L8v368rV5L7afbx-bp22hOT_-zwVwK0XdGctRSWuNaDqhjVQlGACFFUdhsuwUMNRc1o3mIBVqYapOyyVZn3p18DEGtO0U3ADh0HLWHsm1mVx7JtdmcjnxcEr4efrX_AdR9XVz</recordid><startdate>20240523</startdate><enddate>20240523</enddate><creator>Dirim, Ahmet Burak</creator><creator>Namazova, Nazrin</creator><creator>Dirim, Merve Guzel</creator><creator>Oto, Ozgur Akin</creator><creator>Artan, Ayse Serra</creator><creator>Hurdogan, Ozge</creator><creator>Ozluk, Yasemin</creator><creator>Yazici, Halil</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20240523</creationdate><title>622 Baseline inflammatory indexes and clinicopathological features to predict the outcome of acute interstitial nephritis</title><author>Dirim, Ahmet Burak ; Namazova, Nazrin ; Dirim, Merve Guzel ; Oto, Ozgur Akin ; Artan, Ayse Serra ; Hurdogan, Ozge ; Ozluk, Yasemin ; Yazici, Halil</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1160-212a1f327bdf1e63ffd29b2cd364adaa6e51e2dadab6a0ec1379c1a36ec2d5bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dirim, Ahmet Burak</creatorcontrib><creatorcontrib>Namazova, Nazrin</creatorcontrib><creatorcontrib>Dirim, Merve Guzel</creatorcontrib><creatorcontrib>Oto, Ozgur Akin</creatorcontrib><creatorcontrib>Artan, Ayse Serra</creatorcontrib><creatorcontrib>Hurdogan, Ozge</creatorcontrib><creatorcontrib>Ozluk, Yasemin</creatorcontrib><creatorcontrib>Yazici, Halil</creatorcontrib><collection>CrossRef</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dirim, Ahmet Burak</au><au>Namazova, Nazrin</au><au>Dirim, Merve Guzel</au><au>Oto, Ozgur Akin</au><au>Artan, Ayse Serra</au><au>Hurdogan, Ozge</au><au>Ozluk, Yasemin</au><au>Yazici, Halil</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>622 Baseline inflammatory indexes and clinicopathological features to predict the outcome of acute interstitial nephritis</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><date>2024-05-23</date><risdate>2024</risdate><volume>39</volume><issue>Supplement_1</issue><issn>0931-0509</issn><eissn>1460-2385</eissn><abstract>Abstract
Backgrounds-and-aims
Acute tubulointerstitial nephritis(AIN) is a rare cause of acute kidney injury(AKI). We aimed to investigate the characteristics of AIN patients and predictive factors for treatment response.
Method
31 patients diagnosed with AIN by biopsy between 2006-2021 were included in this retrospective study. Baseline clinical, pathological, and laboratory findings, including CBC(complete blood count), creatinine, serum-immune-inflammation-index(SII), neutrophil-to-lymphocyte ratio(NLR), and platelet-to-lymphocyte ratio(PLR) were evaluated. Also, treatment response and creatinine levels at the last follow-up were noted.
Results
Median age was 46 years, and 80.6% of the patients were female. Median baseline creatinine and proteinuria levels were 4.1 mg/dL and 0.84 g/g or g/day. Median follow-up was 14 months. 93.5% of patients received immunosuppressives. End-stage-kidney-disease(ESKD) developed in five patients. Renal recovery(creatinine < 1.4 mg/dL) was observed in 17 (54.8%) patients. Global glomerulosclerosis percentage, interstitial fibrosis(IF), tubular atrophy(TA), granuloma formation, and higher baseline hemoglobin levels were associated with poor renal outcomes(non-responder). Also, ESKD-developed patients had higher baseline hemoglobin(p = 0.033) and lymphocyte(p = 0.044) and lower PLR levels(p = 0.016), as well as higher degrees of global glomerulosclerosis(p = 0.014), IF(p = 0.042), and TA(p = 0.030).
Conclusion
Treatment rates are low for AIN, which may lead to ESKD. Besides chronicity in pathology specimens, higher baseline hemoglobin levels and lower PLR might be prognostic for AIN. Further studies should be conducted on new markers for AIN.
Table:
Baseline clinical/laboratory/pathology and treatment data of responder(last serum creatinine < 1.4 mg/dL) and non-responder groups.
No Response
Responder
Parameters
(n = 14)
(n = 17)
p-value
Age, median (min-max)
44 (21-61)
44.5 (17-71)
0.874
Sex, F/M
10/4
15/2
0.370
Creatinine (mg/dl)
3.8 (2.4-9.1)
4.32 (1.03-11.2)
0.677
eGFR (CKD-EPI)
16.9 (4.7-32)
11.29 (3.69-70)
0.525
Albumin, mean ± std
3.9 ± 0.8
4.0 ± 0.4
0.573
Hgb
11.8 (6.9-13.8)
9.75 (7.2-11.7)
0.029
Lymph
1400 (400-3300)
1180 (500-1700)
0.140
Neutroph
6500 (3100-24700)
5650 (3270-9900)
0.665
Plt
280000 (75000-645000)
291500 (148600-507000)
0.733
Eos
200 (0-700)
135 (0-300)
0.151
SII
1400 (513.6-5689.8)
1635 (495.7-4563)
0.603
NLR
4.88 (2.3-17.6)
4.97 (2.6-12.6)
0.603
PLR
194.3 (124.2-1123.5)
302.26 (151.6-460.9)
0.225
Proteinuria
0.84 (0-8)
0.84 (0-3)
0.766
Follow-up (months)
14 (1-52)
10.5 (2-168)
0.402
Treatments, (%)
Steroids, including pulse
(92.9)
(94.1)
1.000
AZA/MMF
(21.4)
(0)
0.304
Pulse-steroids
(28.6)
(17.6)
0.671
Hemodialysis-at-admission
(28.6)
(17.6)
0.671
AIN Etiology, (%)
Unknown, (50)
Unknown, (23.5)
0.153
NSAID, (14.3)
NSAID, (29.4)
0.412
Antibiotic, (7.1)
Antibiotic, (35.2)
0.094
Sarcoidosis, (21.4)
Sarcoidosis, (5.9)
0.304
Sjögren, (7.1)
Sjögren, (5.9)
1.000
Tubulitis, (%)
Not significant (NS)
(21.4)
(11.8)
0.467
Mild
(57.1)
(88.2)
Moderate
(7.1)
(0)
Severe
2 (14.3)
0 (0)
Lymphocytic infiltration, (%)
NS
(7.1)
(0)
0.452
Mild
(64.3)
(82.4)
Mod
(21.4)
(11.8)
Sev
(7.1)
(5.9)
Eosinophilic inf, (%)
NS
(57.1)
(52.9)
0.815
Mild
(21.4)
(88.2)
Mod
(7.1)
(5.9)
Sev
(14.3)
(11.8)
Plasmacytic inf, (%)
NS
(57.1)
(82.4)
0.124
Mild
(7.1)
(0)
Mod
(7.1)
(0)
Sev
(28.6)
(17.6)
Granuloma formation, (%)
No
(50)
(100)
0.012
Mild/microgranuloma
(28.6)
(0)
Moderate
(14.3)
(0)
Extensive
(7.1)
(0)
TA, (%)
NS
(28.6)
(76.5)
0.024
Mild
(64.3)
(23.5)
Mod
(7.1)
(0)
Sev
(0)
(0)
IF, (%)
NS
(57.1)
(94.1)
0.047
Mild
(35.7)
(5.9)
Mod
(7.1)
(0)
Sev
(0)
(0)
Global sclerotic glomeruli (%), median
(0-83.3)
(0-50)
0.013
Segmental sclerotic glomeruli (%), median
0 (0-9)
0 (0-0)
0.270</abstract><pub>Oxford University Press</pub><doi>10.1093/ndt/gfae069.420</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0931-0509 |
| ispartof | Nephrology, dialysis, transplantation, 2024-05, Vol.39 (Supplement_1) |
| issn | 0931-0509 1460-2385 |
| language | eng |
| recordid | cdi_crossref_primary_10_1093_ndt_gfae069_420 |
| source | OUP_牛津大学出版社现刊 |
| title | 622 Baseline inflammatory indexes and clinicopathological features to predict the outcome of acute interstitial nephritis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T15%3A43%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-oup_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=622%20Baseline%20inflammatory%20indexes%20and%20clinicopathological%20features%20to%20predict%20the%20outcome%20of%20acute%20interstitial%20nephritis&rft.jtitle=Nephrology,%20dialysis,%20transplantation&rft.au=Dirim,%20Ahmet%20Burak&rft.date=2024-05-23&rft.volume=39&rft.issue=Supplement_1&rft.issn=0931-0509&rft.eissn=1460-2385&rft_id=info:doi/10.1093/ndt/gfae069.420&rft_dat=%3Coup_cross%3E10.1093/ndt/gfae069.420%3C/oup_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/&rft_oup_id=10.1093/ndt/gfae069.420&rfr_iscdi=true |